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Controlling Smad4 signaling with a Wip.
EMBO Reports ( IF 6.5 ) Pub Date : 2020-03-18 , DOI: 10.15252/embr.202050246
Peter Ten Dijke 1 , David Baker 1
Affiliation  

Members of the transforming growth factor-β (TGF-β) family play key roles in embryogenesis and in maintaining tissue homeostasis, and their perturbation can result in a broad range of diseases. One way TGF-β family signaling pathways are kept in check is by reversible (de)phosphorylation of intracellular Smad effectors. In this issue of EMBO Reports, Park et al [1] identify the phosphatase wild-type p53-induced phosphatase 1 (Wip1) as a negative regulator of TGF-β family signaling. Mechanistically, Wip1 constrains TGF-β family signaling through direct dephosphorylation of Thr277, an activating MAP kinase phosphorylation site located in the linker region of the common mediator Smad4.

中文翻译:

使用Wip控制Smad4信令。

转化生长因子-β(TGF-β)家族的成员在胚胎发生和维持组织稳态中起着关键作用,它们的扰动可导致多种疾病。抑制TGF-β家族信号传导途径的一种方法是通过细胞内Smad效应子的可逆(去磷酸化)。在本期《 EMBO报告》中,Park等人[1]将磷酸酶野生型p53诱导的磷酸酶1(Wip1)鉴定为TGF-β家族信号转导的负调节剂。从机械上讲,Wip1通过Thr277的直接去磷酸化来限制TGF-β家族信号传导,Thr277是位于共同介体Smad4的连接子区域的活化MAP激酶磷酸化位点。
更新日期:2020-03-18
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